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What do lungs, tend to do if a force is not applied to them?
- they are elastic, & if force is not applied to expand them they’ll deflate (like a balloon) to ~ the size of a fist
What components of the lungs are responsible for this tendency to collapse (collapsing tendency)?
- ~ 2/3 of the tendency to recoil comes from alveolar surface tension
- ~1/3 of the tendency to recoil comes from elastic fibers in the lung connective tissue (parenchyma) surrounding the alveoli
Lung Surface Tension
- results from electrostatic forces between water molecules lining the inside of alveolar walls
- this force is inversely proportional to the square of the distance between them
- aka the shorter the distance between 2 molecules, the greater the Force
What creates surface tension?
- the fact that water molecules on the surface of a liquid layer are pulled toward other water molecules, but NOT toward the adjacent air interface
- evidenced by ability to float objects (eg. pin) on the top of a beaker of water if they are gently placed inside
What 2 entities are water molecules lining the inner surface of alveoli attracted to?
- 1. epithelial cells (they interact w/ H-bonds of phospholipids in cell membrane)
- 2. each other (other water molecules)
In which direction is the surface tension created by the thin film of water lining an alveolus DIRECTED?
- the CENTER of the alveolus
- this creates a pressure in its interior, which is a function of
- 1. surface tension of the fluid
- 2. radius of sphere
- unless opposed this force can collapse the alveoli (small spheres more so than large ones)
What happens to the amount of pressure required to keep an alveoli inflated as the size of the alveolus decreases?
- the collapsing force in GREATER in small spheres (alveoli) b/c the water molecules are closer together
- as alveoli get SMALLER, MORE pressure is required to prevent one from collapsing or to expand it
- the larger a sphere is the farther apart water molecules are - attractive force between water molecules decreases
- decreases water-water interactions, therefore LOWERS surface tension
- is a mixture of lipids & proteins + the major component Dipalmitoylphosphatidyl choline (a detergent - has a hydrophobic & hydrophilic part)
- is secreted by type II alveolar epithelial cells into the inside of alveoli (where water is)
What happens if surfactant ISN’T produced?
- the surface tension of an alveoli is so great that a newborn baby won’t be able to expand their lungs (takes too much force/pressure)
- will become cyanotic - turn blue b/c they’re unable to breathe
- treatment: positive pressure ventilation or use surfactant aerosol spray through nose
What happens if there is a constant surface tension between a larger and smaller alveolus connected by a common airway?
- smaller alveoli have a tendency to collapse INTO larger ones
- surfactant allows the surface tension to vary w/ the radius → tends to equalize the Tension in both alveoli → preventing collapse
- *surfactant allows many differently-sized alveoli to CO-EXIST w/o one collapsing into another due to differences in pressure required to keep each open
- if you look at a typical alveolus it’s tethered by connective tissue (collagen fibers, etc.) & to other alveoli
- alveoli are prevented from collapsing by being “tethered” to each other by the collagen fibers in the interstitium
- therefore neighboring alveoli hold each other open
- the change in volume as transmural pressure is changed
- (change in volume per change in pressure)
- ΔV/ ΔPtm
- what happens to volume as you increase (or decrease) pressure
pressure inside something (eg. balloon) in contrast to the pressure outside
Compliance of a Balloon
- balloons have compliance - the fact that they expand (↑ vol) as you increase their pressure is a measure compliance
- compliance curves for 3 balloons show that for the SAME Ptm, the volume depends upon the STIFFNESS of the balloon walls
- stiff balloon shows low compliance
- floppy balloon shows high compliance
High v. Low Compliance
- a balloon w/ high compliance will achieve a smaller volume at a given amount of Ptm than a balloon w/ low compliance
- a low compliance balloon is more easily blown up (achieves a greater volume) at a given Ptm than a high compliance balloon
What happens as volume increases & balloon walls approach maximum stretch?
the compliance DECREASES (slope becomes less steep…peters off)
Excised Lung Inside Sealed Container Experiment
- lung is expanded by increasing vacuum on outside of the lung (withdrawing air), then the volume is determined
- curve = inflation of lung (↑ vol) by surrounding it w/ negative pressure
- compliance curves are non-linear - reflects how elastic recoil properties of the lung change as a function of volume
What is the relationship between lung volume & the ability for said lung to expand (distend)?
- lungs distend EASILY at lower lung volumes (when small)
- lungs become increasingly stiff at HIGHER volumes (when expanded) as collagen fibers resist further change
- a phenomenon that describes how a lung inflation curve differs from a deflation curve - the 2 won’t be superimposed on one another
- reason: it’s easier to DEFLATE an already inflated alveolus than it is to increase it’s volume when it starts out relatively deflated
Comparison of Air-filled & Saline-filled Lung
- at very low lung volumes compliance is low b/c of HIGH alveolar surface tension (Law of LaPlace)
- once the alveoli begin to expand surface tension ↓ & compliance ↑ until the lungs approach TLC (total lung capacity) & their walls stiffen
- deflation curve DOESN’T show same slope b/c a greater pressure is needed to open a previously closed airway than to keep an open airway from closing
- shows you how much pressure you need to overcome surface tension when you start w/ alveoli that are basically at a minimal volume (empty)
What does inflating the lungs with Saline (fluid instead of air) do?
- it reveals the contribution of alveolar surface tension to the total compliance
- aka eliminates the surface tension component of compliance
- abolishing the air-water surface tension ↑ compliance & ↓ hysteresis
- the lung is very compliant when surface tension is removed
- (emphasized S.T. > elasticity when evaluating lung balloon properties)
How is compliance evaluated in vivo?
by using an esophageal balloon to determine the intrapleural pressure & measuring lung volume at many points during both inspiration & expiration
How does pulmonary disease affect compliance?
- Fibrosis (results from repeated pulmonary infections w/ resulting scarring & proliferation of connective tissue) REDUCES compliance & increases the work needed to expand the lungs
- diseases that destroy lung parenchyma including elastic tissues (eg. emphysema) REDUCE the recoil tendency of the lung & INCREASE compliance
What can inflate the lungs? (2)
- 1. positive pressure: blowing them up from pressure applied to trachea
- 2. applying negative pressure to the outside surface to suck them against the inner chest wall
- this is the way lungs are normally inflated
What causes the 2 pleura to come together?
- serous fluid secreted by both the visceral (inner) & parietal (outer)
- this is what causes the lung to be PULLED against the inner chest wall (i.e. surface tension)
- pleural cavity is normally nonexistent (pathological if it exists in real life)
Transmural (Trans-pulmonary) Pressure
- Ptm = Palv – Pip
- keeps lungs expanded within the thoracic cavity
- recoiling tendency of the lungs is balanced by the outwardly-directed recoil of the chest wall
- if the normally sealed pleural cavity is opened to the atmosphere, air flows IN b/c intrapleural pressure is sub-atmospheric (-3 mmHg)
- the lung will collapsed to its unstretched size
- P1V1 = P2V2
- describes pressure-volume relationships
- increasing the size of a container w/ a set amount of gas → molecules have more room to move → decreased pressure (INHALING)
- reducing the size of a container containing a set amount of gas → molecules pushed closer together → increased pressure (EXHALING)
When is Palv equal to Patm?
- at Functional Residual Capacity (FRC)
- Intraparietal Pressure (Pip) is ~ -5 mmHg
Functional Residual Capacity (FRC)
- the volume of air present in the lungs, specifically the parenchyma, at the END of passive expiration
- at FRC, elastic recoil forces of the lungs & chest wall are equal but opposite & there is no exertion by the diaphragm or other respiratory muscles
Process of Inspiration
- contraction of the diaphragm & the External Intercostals expands the chest wall
- the Pip DROPS → increasing the Ptm, & the lung is pulled outward
- as a result alveoli expand & their pressure drops below Patm (Boyle’s Law)
- this allows air to flow into the lung
What ultimately causes air to flow into & out of the lungs?
- pressure gradients, b/c the average Palv = Patm
- this isn’t conducive to airflow
during inspiration, the increased alveolar volume causes Palv
to drop from 760 → ~758 mmHg
this pressure gradient means air will flow from the atmosphere into the lungs
during expiration, alveolar compression decreases their volume & Palv
rises to ~ 762 mmHg
- this forces air out of lungs back into the atmosphere
What is the primary muscle of respiration in quiet breathing?
- the diaphragm
- separates the thoracic from the abdominal cavity
- all by itself the diaphragm can account for ~65% of tidal volume (how much room the diaphragm makes when it contracts)
What does contraction of the External Intercostals do?
- muscle fibers run “down” & diagonally “in” toward sternum
- (↘ ↙)
- when they contract they rotates ribs 2 → 10 upward & outward INCREASING the A-P (anteroposterior) diameter [makes the chest more “barrel-like”] & stiffening the rib cage against increasing Pip
What accessory muscles become active during more active breathing?
- the scalenes & sternocleidomastoids
- Scalenes: lift the first 2 ribs
- Sternocleidomastoids: lift the sternum
Combined actions of the diaphragm, external intercostals, & scalenes do WHAT?
- give you 500 cc’s the thoracic cavity has to increase by to accommodate the tidal volume
- relaxation of these muscles are responsible for relaxation of the chest during exhalation
Expiration is normally a _______ process driven by the _____ ______ of the lungs.
- Expiration is normally a PASSIVE process driven by the ELASTIC RECOIL of the lungs
- just driven by relaxation of the normal respiratory muscles
- involves contraction of Abdominals & the Internal Intercostals (↖ ↗ orientation)
- abdominals force the diaphragm UPWARD
- internal intercostals DEPRESS the ribs (pull them together) & DECREASE A-P diameter
- overall size of the thoracic cavity is decreased
- active = during talking, exercise, coughing, sneezing, etc. or in diseases w/ increased airway resistance
How does ventilation increase with increasing physical activity? (2)
- 1. increasing breathing frequency
- 2. increasing tidal volume by including inspiratory & expiratory reserve volumes in each breath
What happens to breathing & lung capacity when we start to exercise?
- overall ventilation increases by increasing respiratory rate & depth
- when you start exercising the tidal volume grows b/c you’re ‘digging’ into inspiratory & expiratory reserve (called that b/c they’re the amount you can access when you breath more deeply)
What happens when breathing frequency increases?
- the Tidal Volume DECREASES
- this is b/c the time available for filling & emptying the lungs decreases
- forced expiratory volume in 1 second
- if healthy, a person should be able to blow out ~80% of total vital capacity in the 1st second of forced expiration
forced vital capacity
FEV1/FVC: How to Assess Airway Resistance (another pulmonary function test)
- 1. patient fills lungs to vital capacity; this is FVC
- 2. patient is instructed to forcefully expire; volume of air expired in the 1st second = FEV1
- 3. FEV1/FVC should be 80% or better in a normal subject; less than 80% indicates airway OBSTRUCTION (obstructive pulmonary diseases)
- obstructive diseases (COPD, asthma) blocks or decreases airway radius → unable to breath out 80% of vital capacity
- patient starts w/ full lungs (TLC)
- exhales forcefully until cannot blow out any more air (RV, Residual Volume)
- record volumes of gas that’s exhaled as a function of time
- when the lungs are really fully the amount of gas coming out is large per unit time
- as the lung becomes more empty, the rate of emptying gets smaller & smaller
- volume exhaled = vital capacity
- slope of volume v. time plot = ΔV/ΔT = flow of air at any time
When is air flow greatest according to a volume-time plot?
- flow is GREATEST at the beginning of the exhalation when the lung volume is high
- flow slows as RV is approached (when no more air can be blown out; Residual Volume)
What does a graph of Flow-volume Loop demonstrate?
- maximal expiratory flow for all lung volumes during the forced expiration from TLC to RV
- it shows that flow diminishes as lung volume decreases
- obtained when flow from the slope of a volume-time plot (ΔV/ΔT) is replotted against the absolute lung volume at each point
- starting w/ a full lung flow rises however as most of the air is force out flow of air out decreases
What factors affect expiratory flow?
- generally elastic recoil of the lung
- 1. the stretch of the lung tissue: the greater the stretch, the larger the recoil force
- 2. stiffness of the chest wall
- 3. expiratory muscle forces
- these 3 are GREATEST at TLC & subsequently decrease as lung volume decreases
- 4. alveolar surface tension forces
What do airway diameters vary with?
- airway diameters vary w/ the size of the lung
- larger lung volumes tend to “pull” airways open, decreasing their resistance
- in a forced expiration beginning at TLC the pressure in the airways = pressure in the pleural space
What happens as air leaves the lung during a forced expiration?
the pressure in the airways drops to the “equal pressure point” (EPP) where airway pressure = pleural pressure
What happens if the pressure in the airways drops below the EPP?
smaller airways are compressed & airflow is LIMITED
Full Flow-volume Plot
- has maximum expiration from TLC to RV & inspiration from RV
- by convention, expiratory flow is positive & inspiratory flow is negative
- in quiet breathing the volume varies between the inspiratory capacity & functional residual capacity
Full Flow-volume Plot in Emphysema
- emphysema reduces expiratory flow at ALL lung volumes b/c it narrows airways & causes a loss of elastic recoil in the damaged lung tissue
- this leads to a reduced driving pressure
- much harder to expire air
- also loss of many alveoli → less alveolar surface tension, further reducing capacity to fully exhale
What 2 entities may be increased in emphysema?
- TLC (total lung capacity) - no elasticity means lungs can expand further
- RV (residual volume) - also means lungs can’t contract as effectively; more air remains after expiration
- this occurs from a loss of recoil